Run for Your Life Flashcards
1
Q
Label the Diagram
A
2
Q
Describe the role of tendons.
A
Attach muscle to bones. Enable muscles to power joint movement. Not elastic. Made of white fibrous tissue - bundles of collagen fibres so strong.
3
Q
Describe the role of ligaments.
A
Holds the position of bones and controls and restricts movement in the joint. Made of yellow elastic tissue and collagen which gives both strength and elasticity and flexibility. Connects bone to bone.
4
Q
Describe the role of cartilage.
A
Cartilage protects bones within joints. Hard but flexible. Elastic and able to withstand compressive forces. Made of cells called chondrocytes within an organic matrix of collagen fibres. Very good shock absorber. 2 types: hyaline cartilage and white fibrous cartilage.
5
Q
Describe the role of bone.
A
Supports the body structure and protect vital organs, strong and hard.
Bone cells embedded in a matrix of collagen fibres and calcium salts is light. Very strong under compression forces.
6
Q
Describe the role of synovial fluid.
A
Acts as lubricant
7
Q
Describe how a pair of antagonistic muscles work to move a joint.
A
The pair of muscles create opposite forces. When one relaxes (stretches), the other contracts (shortens).
8
Q
What are the extensor and flexor muscles?
A
- Extensor muscle: the muscle which contracts to extend the joint.
- Flexor muscles: The muscle which contracts to flex/ bend the joint/ limb.
9
Q
What are the 3 main types of muscle?
A
- Smooth muscle
- Cardiac muscle
- Striated, Voluntary or Skeletal Muscle
10
Q
Describe smooth muscle.
A
Under the control of the involuntary nervous system. Causes slow contractions of many internal organs, i.e. arteries, intestine. Long and spindle shaped cells, each with their own nucleus. No striations/stripes (parallel groves). Contractions are slow & long lasting, and the fibres fatigue very slowly.
11
Q
Describe cardiac muscle.
A
Only found in the heart. Striated/striped muscle. Interconnected fibres to ensure a co-ordinated wave of contraction. Contracts spontaneously (myogenic). Does not fatigue. Capable of short contractions over a long time period (your whole life).
12
Q
Describe Striated, Voluntary or Skeletal Muscle.
A
Muscle attached to the skeleton & involved in locomotion.
Under the control of the voluntary nervous system. It contracts rapidly, but fatigues quickly. Capable of strong contractions.
13
Q
Describe the muscle tissue.
A
Muscle is made up of bundles of muscle fibres, surrounded by connective tissue. Each muscle fibre is one cell which is multinucleate and striated. Inside the muscle fibre cell are numerous myofibrils. Each myofibril is composed of repeated contractile units called sarcomeres. The two types of protein within these are actin and myosin.
14
Q
Describe what happens when muscle contracts.
A
Contractions are brought about by co-ordinated sliding of the protein filaments over each other in the sarcomere. The actin moves between the myosin. This shortens the length of the sarcomere, and hence the length of the muscle.
15
Q
Why do muscles appear striped (striated) under the microscope?
A
The actin and myosin overlap. Where actin filaments occur on their own, there is a light band on the sarcomere. Where myosin filaments occur on their own, there is an intermediate-coloured band. Where both actin and myosin filaments occur, there is a dark band.
16
Q
Define sarcoplasm.
A
The cytoplasm of a muscle cell.
17
Q
Describe the sequence of events that occurs at the neuromuscular junction.
A
A nerve impulse arrives from a motor neurone. Acetylcholine is released from the end of the neurone. Acetylcholine results in the release of calcium ions (Ca2+) from the sarcoplasmic reticulum. Ca2+ diffuse into the sarcoplasm surrounding the myofibrils.
18
Q
Describe the Sliding filament theory.
A
Nerve impulses at a neuromuscular junction release Ca2+ ions from the sarcoplasmic reticulum. These diffuse through the sarcomere. Ca2+ ions attach to troponin on the actin causing tropomyosin to shift position and expose myosin binding sites. Myosin heads bind with binding sites and form cross bridges. This releases ADP and Pi. Myosin changes shape and the myosin head moves forward. Actin moves over the myosin.
ATP binds to myosin causing the head to detach. ATPase hydrolyses ATP to ADP and Pi changing the shape of the myosin head and returning the myosin head to it’s previous position.
19
Q
Describe what happens when the muscle relaxes.
A
The muscle is no longer stimulated by the motor neurone. Ca2+ is pumped back into the sarcoplasmic reticulum by active transport. This requires ATP. The troponin moves back to its original position and the tropomyosin moves to back to cover and block the myosin binding sites on the actin.
20
Q
Describe what happens to muscles in rigor mortis.
A
After death, ATP production stops. With an absence of ATP, the myosin heads will remain attached to the actin (the cross-bridges stay intact). The muscle is unable to relax and remains ridged. The cross-bridges are only broken when the muscle fibres start decomposing.
21
Q
Describe the role of calcium ions in the contraction of skeletal muscles.
A
- Calcium ions released in response to nervous stimulation of the muscle set up contraction of the sarcomeres
- Calcium ions bind to troponin changing the shape of the molecule
- This change in shape pulls the tropomyosin away from the myosin binding sites on the actin molecules exposing them
- The myosin heads now bind, setting up the contraction
- Calcium ions are also needed for the action of the ATPase enzyme in the myosin heads, which enables the heads to return to their original resting position
22
Q
Explain why the presence of ATP and it’s hydrolysed form are so important for the contraction of striated muscle.
A
- The ATP binds to the myosin head, and the release of energy when it is hydrolysed allows the head to return to the resting position
- The bonding of ADP and Pi results in changes in the shape of the myosin head so it can bind to the actin binding site
- The release of the ADP and Pi results in another shape change which results in the bending of the myosin head causing the actin to slide over the myosin
- ATP is also needed as the energy supply for the calcium pump which returns calcium ions to the sarcoplasmic reticulum, ending the contraction.
23
Q
Write the overall word and balanced chemical equation for respiration.
A
Glucose + Oxygen –> Carbon Dioxide + Water + energy
C6H12O6 + 6O2 –> 6CO2 + 6H2O + 38 ATP
24
Q
Draw a mitochondrion
A
25
What are the 5 processes in Aerobic Respiration?
* Glycolysis
* The Link Reaction
* Krebs Cycle
* The Electron Transport Chain
* ATP synthesis & Chemiosmosis
26
Where in the cell does glycolysis occur?
In the cytoplasm (or sarcoplasm of muscle cells).
27
What substrate is needed for Glycolysis and where does it come from?
Needs glucose (hexose monosaccharide) as substrate.
* Could come straight from bloodstream.
* Glycogen in muscle or liver cells is converted to glucose.
28
Describe Glycolysis
1. Glycogen is rapidly hydrolysed
2. Glucose (6C) is phosphorylated using the 2 phosphates released from the hydrolysis/ dephosphorylation of 2x ATP. The hydrolysis releases energy and the phosphates are transferred between the molecules by a kinase enzyme. The phosphorylated glucose then splits to form 2 intermediate (3C) compounds (GALP) each with a phosphate attached.
3. Each GALP is oxidised/dehydrogenated to form 1 molecule of pyruvate (3C). The 2 hydrogen atoms removed from each GALP are used to reduce 1 molecule of NAD to form reduced NAD or NADH + H+.
4. Each GALP is also dephosphorylated. The phosphate is used to phosphorylate one molecule of ADP to form ATP - known as substrate-level phosphorylation. The reaction requires a kinase enzyme. In total 4 ATP are made, however 2 are used in the first step so there is a net gain of 2 overall.
29
Describe the link reaction.
1. Pyruvate is decarboxylated and one molecule of CO2 is released
2. Pyruvate is oxidised and dehydrogenated. The 2 hydrogen atoms are used to reduce 1 molecule of NAD to form reduced NAD or NADH + H+
3. 1 molecule of Acetyl CoA (2C) is produced and enters the Krebs cycle
30
Where in the cell does the Krebs cycle take place?
In the mitochondrial matrix.
31
Describe the Krebs cycle.
1. One molecule of Acetyl CoA is combined with Oxaloacetate. The 6C compound Citrate is formed.
2. The 6C compound is decarboxylated and one molecule of CO2 is released
3. The 6C compound is oxidised and dehydrogenated to form the 5C compound (α-Ketogluterate). The 2 hydrogen atoms are used to reduce 1 molecule of NAD to form reduced NAD
4. The 5C compound is decarboxylated and one molecule of CO2 is released
5. 1 molecule of ATP is created by substrate-level phosphorylation
6. The 5C compound is oxidised and dehydrogenated to form a 4C compound (Oxaloacetate). 4 hydrogen atoms are used to reduce 2 molecules of NAD to form 2 molecules of {reduced NAD / NADH + H+}
7. 2 hydrogen atoms are used to reduce 1 molecule of FAD to form reduced FAD. The 4C compound is reformed.
32
Describe the process of ATP synthesis at the electron transport chain.
1. Reduced co-enzyme brings 2 H atoms to the ETC. The reduced co-enzyme is oxidised when it passes its 2 H atoms to the first electron carrier in the ETC.
2. Each hydrogen atom is split into an H+ and an e-. The electrons pass down the ETC between the e- carriers in a series of redox reactions - energy is released.
3. Energy is used to pump H+ ions through the e- carriers into the intermembrane space.
4. As the H+ ions accumulate, an electrochemical gradient is created and the pH of the space falls and becomes acidic.
5. H+ ions diffuse down the electrochemical gradient through a stalked particle back into the mitochondrial matrix. As they diffuse through, they activate ATP synthase which phosphorylates ADP to create ATP in a condensation reaction.
6. To maintain the electrochemical gradient, each H+ ion re-joins with an electron to reform a hydrogen atom. Two hydrogen atoms bond to ½O2 to form one molecule of water (2H+ + 2e- + ½O2 -> H2O).
The oxygen acting as the final electron acceptor on ETC is reduced.
This method of ATP synthesis is called **oxidative phosphorylation**.
33
Describe what happens if there is a lack of oxygen in the mitochondrion.
Effect on the electrons: (think about oxygen)
1. Without oxygen, there is no final electron acceptor for the electron transport chain. The electrons are unable to leave the final electron carrier. Electrons cannot move down the electron transport chain and so redox reactions stop and energy is no longer released.
2. Without the movement of electrons, reduced co-enzyme is unable to become oxidised by passing its electrons to the first electron carrier in the electron transport chain. Oxidised co-enzyme (NAD and FAD) is unable to be regenerated and sent back to glycolysis, the link reaction and the Krebs cycle. Without oxidised NAD and FAD, these three processes stop and ultimately aerobic respiration stops.
Effect on the hydrogen ions:
1. Without oxygen, the H+ ions that have diffused down through the stalked particle have no molecule to bind to. Therefore, as they start to accumulate in the matrix the electrochemical gradient disappears and no further H+ ions diffuse down through the stalked particle.
2. Without the energy from the redox reactions, H+ ions are not pumped into the intermembrane space and so no electrochemical gradient is created. Therefore, H+ ions do not diffuse down through the stalked particle.
As a result of steps 1 and 2, ATP synthase is unable to phosphorylate ADP to create ATP. ATP production stops.
34
Explain the role of carrier molecules in the electron transport chain.
* Recieve hydrogen from reduced NAD/ FAD.
* Break hydrogen into H+ and electrons.
* Electrons are transferred by a series of redox reactions.
* The energy is used to pump H+ into the intermembrane space.
35
What is the effect on aerobic respiration of oxygen demand in cell excedding the supply.
Without oxygen to accept the H+ ions and electrons (act as the final electron acceptor), the electron transport chain stops. The reduced NAD produced in glycolysis, link reaction and Krebs cycle are not able to be oxidised.
36
What affects the rate of respiration?
* high levels of ATP or citrate inhibits kinase enzyme
* low levels of ATP or citrate leads to high levels of ADP which activates kinase enzyme
* End-point inhibtion
* Absence of oxygen
* Absence of H+ ions.
37
Describe the process of Anaerobic Respiration. (Involves glycolysis)
1. Glucose --> 2 intermediate (3C) compounds (GALP). Each GALP is oxidised to form 1 molecule of pyruvate. 2H atoms are removed per GALP.
2.The 4 H atoms removed reduce 2 molecules of NAD to form 2 reduced NAD
3. Each reduced NAD is oxidised and 2 molecules of pyruvate are reduced to form 2 molecules of lactate (lactic acid).
4. The oxidation of reduced NAD reforms NAD. This can then be used to receive further hydrogen atoms from the oxidation of GALP. This keeps glycolysis going.
5. The continued break down of glucose to pyruvate enables the formation of a net gain of 2 ATP per molecule of glucose by substrate level phosphorylation.
38
Describe the consequence of lactate accumulating in cells.
Lactate forms lactic acid in solution. This reduces the pH of cells. The enzymes that catalyse glycolysis are inhibited and glycolysis stops. Muscle contraction and physical activity stops.
39
Describe the effect of the products of anaerobic respiration on enzymes.
The H+ ions from lactic acid accumulate in the cytoplasm. They neutralise the negatively charged R groups of amino acids in the active site of an enzyme. This prevents the substrate being attracted to, and binding to the active site. Enzyme substrate complexes can’t form.
40
How is lactate removed?
Lactate moves into the blood and is transported to the liver. It is oxidised and converted back to pyruvate. The pyruvate is then fully oxidised via the link reaction, Krebs cycle and the electron transport chain to form CO2 and water. Some pyruvate can be converted back into glucose and transported back to the muscles to be stored as glycogen (gluconeogenesis). This is known as the Cori cycle.
41
What is the excess O2 requirement after exercise known as?
The oxygen debt or post-exercise oxygen consumption (sometimes EPOC)
42
What is aerobic capacity?
The ability to take in, transport and use oxygen.
43
What are the 2 types of skeletal muscles?
* Fast twitch muscle fibres
* Slow twitch muscle fibres
44
Describe fast twitch muscle fibres (role).
* Specialised for rapid, intense contractions
* The ATP used in these contractions is produced almost entirely from anaerobic respiration.
45
Describe slow twitch muscle fibres (role).
* Specialised for slower, sustained contraction.
* Can cope with long periods of exercise
* Carry out a large amount of aerobic respiration.
46
List the characteristics of fast twitch muscle fibres.
* Pale pink/ white
* Few capillaries
* Little myoglobin
* Large glycogen stores
* Lots of sarcoplasmic reticulum
* Fatigue easily
* Few mitochondria
47
List the characteristics of slow twitch muscle fibres.
* Deep red
* Lots of capillaries
* Lots of myoglobin to store O2
* Not much stored glycogen
* Little sarcoplasmic reticulum
* Doesn't fatigue easily
* Many mitochonidra
48
What is myoglobin?
* Protein similar to haemoglobin - made of 1 chain rather than 4
* It has a much higher affinity for oxygen than haemoglobin
* Acts as an oxygen store in muscles
* Dark red in colour which gives slow twitch muscle fibres their distinctive colour.
49
What happens during exercise?
* Breathing rate/ ventilation rate increases
* Breathing depth increases
* Cardiac output increases
50
Describe inhalation.
Intercostal and diaphragm muscles contract. Volume increases, ribs move up, diaphragm moves down, low pressure.
51
Describe exhalation.
Stretch receptors are stimulated and send inhibitory impulses. Causes elastic recoil. Internal intercostal muscles contract. Volume decreases, ribs move down, diaphragm moves up, high pressure.
52
Name the region of the brain that controls breathing.
The ventilation centre in the medulla oblongata.
53
At rest, state the most important stimulus controlling breathing rate and depth.
The concentration of dissolved CO2 in arterial blood (via the drop in pH).
54
Describe how an increase in exercise brings about an increase in breathing rate and depth.
1. Increase in dissolved CO2 in blood plasma due to increased respiration which creates carbonic acid (H2CO3).
2. Carbonic acid dissociates into hydrogen ions and hydrogen carbonate ions. This lowers the pH of the blood. (CO2 + H2O -> H2CO3 -> H+ + HCO3)
3. Chemoreceptors in the walls of the aortic arch and carotid artery detect the increase in CO2/ drop in pH in the blood. Impulses are sent to the ventilation centre in the medulla oblongata.
4. Chemoreceptors in the ventilation centre of the medulla oblongata can also detect the drop in pH.
5. An increased number of / more frequent impulses are sent from the ventilation centre via a sympathetic neurone to the intercostal muscles & diaphragm to stimulate more frequent and stronger contractions.
55
State the purpose of the more frequent and deeper breaths.
This maintains a steep concentration gradient of CO2 between the alveolar air and the blood. This ensures efficient removal of CO2 from the blood and uptake of O2 into the blood.
56
Describe the other stimuli that will increase breathing rate and depth when starting exercise.
1. The motor cortex of the brain controls movement. As soon as exercise begins impulses from the motor cortex are sent to the ventilation centre in the medulla oblongata.
2. Stretch receptors (mechanoreceptors) in tendons and muscles involved in movement send impulses to the ventilation centre.
3. Temperature receptors (thermoreceptors) detect the increase in blood temperature and send impulses to the ventilation centre.
4. Chemoreceptors detect a drop in O2 concentration in the blood and send impulses to the ventilation centre. These are rarely stimulated under normal circumstances.
57
What is the control of CO2 concentration an example of?
Homeostasis operating via negative feedback.
58
State the name of the equipment used to measure lung volumes.
Spirometer
59
Define tidal volume.
The volume of air that is breathed in and out in one breath
60
Define vital capacity.
The maximum volume of air a person can inhale and exhale
61
Define breathing rate.
The number of breaths in a set time period. Measured in breaths per minute.
62
Define minute ventilation.
The volume of air taken into the lungs in one minute.
63
Describe how to calculate tidal volume.
Measure the vertical distance between a peak and trough. Convert to a volume using the calibration scale. Measure multiple breaths to calculate a mean average.
64
Describe how to calculate vital capacity.
Measure the vertical distance between the highest peak and the lowest trough. Convert to a volume using the calibration scale.
65
Describe how to calculate breathing rate.
Count the number of troughs in a set period of time. Units are breaths min-1.
66
Describe how to calculate minute ventilation rate.
Multiply the (mean) tidal volume (dm3) by the breathing rate (number of breaths per minute). Units are dm3min-1.
67
Describe how to calculate oxygen consumption.
Identify a trough at the start of the trace and a trough a known time period away i.e. 1 minute. Draw a trend line between the 2 troughs. From the second trough, draw a horizontal line back to line up with the first trough – form a triangle. Calculate the difference in volume between the first trough and the horizontal line.
68
Describe how to calculate the rate of oxygen consumption.
Divide the oxygen consumption by the time over which it falls i.e. dm3min-1 or cm3s-1
69
Define myogenic.
The heart muscle can contract without any external nervous stimulation. The stimulation is generated from within the muscle. The stimulation brings about depolarisation of the heart muscle.
70
Describe the process of a heart beat.
1. The sinoatrial node (SAN) generates an electrical impulse that results in a wave of depolarisation spreading over the atria (through the atrial walls) causing them to contract (atrial systole). Blood is forced into the relaxing ventricles.
2. The impulse arrives at the atrioventricular node (AVN) where it is delayed by 0.13 seconds. The rest of the impulse is blocked by the non-conducting layer between the atria and ventricles.
3. After the slight delay, the impulse travels down to the heart apex through the Purkyne fibres in the bundle of His within the septum of the heart.
4. The impulse travels along the Purkyne fibres which branch out within the ventricular muscle. Contraction of the ventricles (ventricular systole) occurs from the apex and travels up in the direction of the atria. This causes the blood to be pushed up and out of the heart through the aorta and pulmonary artery.
71
State the importance of the non-conducting layer between the atria and the ventricles.
Prevents the impulse travelling to the muscle at the top of the ventricles. This would cause the ventricles to contract from the top downwards forcing the blood to the bottom of the heart and not up and out.
72
State why it is important for the impulse to be delayed in the AVN.
This ensures that the atria have finished contracting and that the ventricles have filled with blood before they then contract.
73
State how the electrical activity of the heart can be detected and displayed.
An electrocardiogram (ECG) measures the change in potential difference in heart muscle cells. Measured in millivolts (mV).
74
State what an ECG trace can provide information about
Abnormal heartbeats, areas of heart damage and inadequate blood flow to areas of the cardiac muscle
75
Describe tachycardia and what could cause it.
A heart rate of more than 100 bpm. Could indicate anxiety, fear, fever or exercise. Could also be associated with coronary heart disease, heart failure, use of certain medicines or drugs, fluid loss or anaemia
76
Describe bradycardia and what could cause it.
A heart rate of less than 60 bpm. Could indicate athletic fitness, hypothermia or heart disease, or can be associated with certain medicines or drugs
77
Describe arrythmia and what could cause it.
The normal electrical activity and rhythm of the heart is disrupted which creates electrical disturbances resulting in irregular beats or timings between the beats. Could indicate ischaemia due to atherosclerosis in coronary arteries
78
Name the region of the brain that controls heart rate.
The cardiovascular control centre located in the medulla oblongata
79
Name the part of the central nervous system that helps control heart rate
The autonomic nervous system
80
Describe how an increase in exercise leads to an increase in heart rate.
1. Exercise increases the concentration of CO2 and lactate in the blood. This results in an increase in H+ ions and a decrease in pH.
2. The {increase in H+ concentration / drop in pH} is detected by chemoreceptors in the aortic arch and carotid artery.
3. Impulses are sent to the cardiovascular control centre in the medulla oblongata.
4. Increased frequency of impulses sent {down the sympathetic {nerve/neurone} / via the sympathetic nervous system} to the SAN.
5. The release of noradrenaline results in more frequent stimulation of the SAN and more frequent waves of depolarisation and contraction of the heart muscle.
81
How to calculate cardiac output?
Cardiac output (cm3/min) = stroke volume (cm3) x heart rate (bpm)
82
State what else must increase in order to increase stroke volume
Venous return – the volume of blood returning to the heart. In order to pump more blood per contraction, more blood must return to it!
83
State what else increases along with heart rate and increased cardiac output
Blood pressure
84
Describe how heart rate is prevented from rising too high during exercise or brought back to normal after exercise
1. The increase in blood pressure is detected by baroreceptors in the aortic arch and carotid artery
2. Impulses are sent to the cardiovascular control centre in the medulla oblongata
3. Impulses are sent {down the {parasympathetic/vagus} {nerve/neurone} / via the parasympathetic nervous system} to the SAN
4. Less frequent stimulation of the SAN results in less frequent waves of depolarisation and contraction of the heart muscle – reduction in heart rate
85
What is the role of sympathetic nerve in control of heart rate?
* Accelerator - increase heart rate
* sends increased frequency of impulses to stimulate the SAN so there is more frequent depolarisation.
86
What is the role of parasympathetic nerve in control of heart rate?
* decelerator - decreases heart rate
87
What is the control of heart rate an example of?
Negative feedback in homeostasis
88
Describe the hormonal effects on heart rate
* Fear, excitement and shock cause the release of adrenaline from the adrenal glands located just above the kidneys.
* The adrenaline travels in the bloodstream to the SAN where it has a direct effect to increase SAN stimulation and depolarisation.
* Adrenaline also causes vasodilation of arterioles supplying skeletal muscles and vasoconstriction of arterioles going to the digestive system and other non-essential organs.
* Adrenaline also causes an anticipatory increase in heart rate before a race.
89
Define homeostasis
The maintenance of a stable internal environment within an appropriate range
90
Define negative feedback.
A deviation from the norm results in a change in the opposite direction, back to the norm
91
Define positive feedback.
A deviation from the norm results in the further movement of the condition away from the norm
92
Chemoreceptors
* detect change in CO2, O2, pH
* found in medulla oblongata, aortic arch, carotid artery
93
Thermoreceptors
* detect change in temperature
* found in hypothalamus and skin
94
Baroreceptors
* detect changes in pressure
* found in carotid artery and aortic arch
95
Mechanoreceptor
* detects changes in muscle contraction
96
Detection of an increase in temperature will cause an impulse to be sent to:
Heat loss centre in the hypothalamus (control centre)
97
Describe the mechanisms used to decrease body temperature
* Arterioles – dilate (vasodilation) to increase blood supply to the surface capillaries. The shunt vessel constricts so blood flows closer to the skin. More heat lost by radiation.
* Sweat glands – release sweat to increase heat loss by evaporation.
* Hair erector muscles – relax to lower hairs on skin to prevent a layer of air being trapped.
* Liver – decrease in metabolic reactions (respiration is exothermic).
* Skeletal muscles – relax repeatedly to prevent shivering. (An increase in muscle contraction increases temperature).
* Skeletal muscles – move body to change shape (spread out)
* Diaphragm & intercostal muscles - some animals are known to pant (dogs) causing more evaporation from the mouth.
98
Detection in a decrease in temperature will cause an impulse to be sent to:
Heat gain centre in the hypothalamus (control centre)
99
Describe the mechanisms used to increase body temperature
* Arterioles – constrict (vasoconstriction) to reduce blood supply to the surface capillaries. The shunt vessel dilates so blood flows further from the skin. Less heat lost by radiation.
* Hair erector muscles – contract to raise hairs on skin to trap a layer of air to insulate the body.
* Skeletal muscles – contract repeatedly to cause shivering. Increase in muscle contraction increases temperature.
* Liver – increase in metabolic reactions (respiration is exothermic).
* Skeletal muscles – move body to change shape (curl up), move somewhere warmer
100
Explain why moderate exercise lowers the risk of upper respiratory tract infections (URTIs)
* moderate exercise increases the number + activity of natural killer cells found in blood and lymph
* provide non-specific immunity against cells invaded by viruses and cancerous cells, target cells that are not displaying 'self' markers
* release the protein perforin, which makes pores in the targeted cell membrane so other molecules e.g. proteases can cause apoptosis
* activated by cytokines and interferons
101
Explain why vigorous exercise increases the risk of URTIs
* reduced the numbers of natural killer cell, phagocytes, B cells and T helper cells
* the decrease in T helper cells reduces the amount of cytokines available to activate lymphocytes
* reduces the quantity of antibodies produced
* inflammatory response can occur in muscles due to damage which can reduce availability of non-specific immune response against URTIs
* physical exercise and psychological stress release adrenaline and cortisol which suppress immune system
102
Describe other possible reasons as to why elite athletes suffer more URTIs
* Athletes have an increased exposure to different pathogens at competitions.
* International competitions can expose them to pathogens from other parts of the world
* The mode of travel can expose them to new pathogens i.e. airplanes.
* High contact sports, team sports and staying in the athlete’s village can also aid the transmission of pathogens.
* Athletes can also be under physical and psychological stress, which will cause the release of adrenaline and cortisol – these hormones are known to suppress the immune system.
103
Describe why exercise is important to human health
* Reduction in risk of CVD (CHD & stroke) - Increase in vasodilation which lowers blood pressure. Increases blood HDL levels and reduces blood LDL levels.
* Maintaining a healthy weight – improved energy balance between input and usage preventing obesity. Increased sensitivity of muscle cells to insulin which improves blood glucose regulation leading to a reduced risk of developing type II diabetes.
* Increase in bone density (delays onset and progression of osteoporosis), reduces the risk of some cancers & improves mental wellbeing.
104
Describe the consequences of lack of exercise
Higher risk of weight gain, obesity, type II diabetes, high blood pressure, higher blood LDL levels, lower blood HDL levels, coronary heart disease, stroke, osteoporosis.
105
Advantages of key-hole surgery
* Small number of small incisions made (4mm) –
* less invasive, less damage to surrounding tissue, less risk of bleeding
* less risk of infection, less scaring
* can be performed under local anaesthetic (less anaesthetic needed),
* shorter operation, reduced use of pain killers, shorter stay in hospital,
* shorter recover time
* more patients can be treated in the same time frame
* economic benefit to NHS i.e. cheaper than invasive surgery
106
Explain the advantages and disadvantages of replacing damaged ligaments by tendons.
Advantages: bones held in place within the joint
Disadvantages: the tendon is inelastic so the joint may be less flexible, long physiotherapy period to gradually stretch the tendon, long recovery time
107
Define prosthesis
An artificial body part used by someone with a disability to enable them to regain some degree of normal function or appearance
108
Hormones are made by...
endocrine glands
109
What are the 2 main ways hormones interact with the cell?
* Bind to a complementary membrane-bound receptor on the cell surface
* Directly enter the cell through the cell surface membrane
110
Describe the structure & properties of peptide hormones
Short protein chains of 100 – 300 amino acids in length. The polypeptide chain is folded into the tertiary structure with a specific 3D shape. They are polar and are soluble in water.
111
How do peptide hormones interact with the cell?
The peptide hormone is unable to pass through the phospholipid bilayer of the cell surface membrane. So it binds to its complementary target cell receptor embedded within the cell surface membrane. Formation of the hormone-receptor complex activates a second messenger protein within the cytoplasm. This can be achieved by phosphorylation by the hormone-receptor complex acting as a kinase enzyme. The activated second messenger protein activates a second messenger signalling cascade (signal transduction pathway) to activate transcription factors in the nucleus.
112
Examples of peptide hormones
Growth hormone, insulin, erythropoietin (EPO)
113
Describe the structure & properties of steroid hormones
Formed from lipids. Have complex ring structures. They are hydrophobic, and therefore insoluble in water. They are lipid soluble.
114
How do steroid hormones interact with the cell?
The steroid hormone passes directly through the phospholipid bilayer of the cell surface membrane. It binds to its complementary target cell receptor in the cytoplasm. A hormone-receptor complex is formed. This complex travels to the cell nucleus where it acts as a transcription factor to activate genes and start transcription.
115
Examples of steroid hormones
Testosterone, oestrogen
116
Describe the process of gene activation that initiates transcription
DNA unwinds and activated transcription factors bind to the promoter region upstream of a gene. RNA polymerase then binds, and the transcription initiation complex forms. Hydrogen bonds between the bases then break and transcription begins.
117
Describe the possible ways in which a gene may not be activated
A repressor protein may be bound to the promoter region blocking the attachment of transcription factors. Repressor molecules could also bind to the transcription factors preventing them binding to the promoter. They could also prevent the activation of the transcription factors.
118
Describe the ways in which transcription factor activation may be regulated
Some transcription factors are present in all cells. Some are only synthesised in a particular type of cell or at a particular stage of development. Most are created in an inactive form which will be converted into an active form as a result of a signal transduction pathway being activated by a hormone or growth factor.
119
What is doping?
The use of drugs to enhance performance in sport
120
Describe the mode of action of Erythropoietin
A peptide hormone produced by the kidneys. It stimulates the formation of new red blood cells. The increased number of red blood cells can carry more O2. EPO can be produced using DNA technology and used to treat anaemia.
121
Describe the risks of taking erythropoietin
If EPO levels are too high, too many red blood cells are made. This increases the risk of thrombosis, maybe leading to a heart attack, stroke or even death
122
Describe the mode of action of Testosterone
A steroid hormone produced in the testes of males and adrenal glands in small amounts in both sexes. Binds to androgen receptors and modifies gene expression to increase anabolic reactions such as protein synthesis in muscle cells. Muscles increase in size and strength. Is taken in a synthetic form as an anabolic steroid e.g. nandrolone.
123
Describe the risks of taking testosterone.
Can cause high blood pressure, liver damage, changes in the menstrual cycle in women, decreased sperm production and impotence in men, kidney failure and heart disease. It can increase aggression in both sexes.
124
Describe the mode of action of Creatine.
A nutritional supplement – not banned. An amino acid derived compound. Naturally found in meat & fish, or can be synthesised in the body. Once ingested and absorbed it can increase the amounts of creatine phosphate in muscles. Improvement in repeated, short-duration, high-intensity exercise and increase in muscle mass and strength with heavy weight training. Can improve recovery time from injury.
125
Describe the risks of taking creatine.
Can cause diarrhoea, nausea, vomiting, high blood pressure, kidney damage and muscle cramps.
126
Why do athletes need to be careful if they have medical conditions?
Their prescription drug for their condition may be banned as it could enhance their performance. They will need to gain permission to use it. It is the responsibility of the athlete to check if their medication is banned or not and that they do not take it by accident when they are not supposed to. They can get a medical certificate if they need to take a banned substance.
127
What is meant by absolutism?
All actions are wrong in any circumstance.
128
What is meant by Relativism/ Rationalism?
The action is acceptable if there is an overall benefit to the individual or society or is considered morally acceptable by a particular society.
129
Explain why athletes may take enhancing substances
Elite athletes may have a high social or media status which they want to maintain, they need to maintain or improve their performance for funding from their country or their sponsors, they want to defend their titles or gain new ones, to beat a rival, to reach their coach’s expectations or other team members, they may not be aware that they are taking them.
It is ethically acceptable as athletes have the right to decide for themselves. It levels out the inequality of competition due to differences in time available for training, resources and genetic differences between athletes. A banned substances for a particular sporting discipline, may not be banned for another.
130
Explain why taking enhancing substances is banned
Athletes may not be aware of the risks of taking some enhancing substances so the ban is there to protect them. There may be added costs to the NHS due to treatment of side effects. It is not fair on the other athletes competing alongside them. It ensures that there is a level playing field of competition. If athletes are known take substances it may encourage younger athletes and the general public to take them as it normalises them – they become a poor role model.
131
Explain why athletes decide not to take enhancing substances
An athlete wishes to gain respect and titles due to their hard work. The risk of side effects to their health. It is more important to take part in competition rather than win. They want to be a good role model to young athletes. They can lose their funding, sponsorship or right to compete if they take them.
